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Year 2 - Theme A > Block 9 > Flashcards

Block 9 Flashcards

0
Q

What are basket cells?

A

They surround the base of the hair follicle and sense pressure.

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1
Q

What are the 3 main layers in the skin?

A

Epidermis, dermis, sub cutis

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2
Q

What are merkel cells?

A

They are found at the basal layer of the epidermis and acts as sensory receptors.

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3
Q

What are the 4 layers of the epidermis?

A

Basal layer
Stratum spinosum
Stratum granulosum
Stratum corneum

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5
Q

What are the 2 layers of the dermis and their functions?

A 
There are 2 layers:
Papillary layer (most superficial): thin arrangement of collagen, highly vascular
Reticular layer: collagen fibres are thick and lie parallel to the skin, provides structure and elasticity. Supports sweat glands and hair follicles, contains nerves.
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6
Q

What are the functions of the skin?

A 
Prevents dehydration
Protects the body from toxins
Innate immunity
Protects from UV
Sensory reception
Temperature regulation
Calcium homeostasis
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7
Q

Define a 1st degree burn and how it heals

A

Only affects epidermis - red, no blisters and painful

Dermis supports regeneration of epidermis and the skin gets inflamed to encourage the clean up of cells

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8
Q

Define a 2nd degree burn and how it heals

A

Effects the papillary dermis - Red, blisters and very painful
Some of the skins accessory organs remain - hairs and glands. Epithelial cells that line these structures have the ability to divide and regenerate the epidermis

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9
Q

Define a 3rd degree burn and how it heals

A

All of the dermis is removed - white, no blisters, no pain

Requires a skin graft to heal - strong risk of infection

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10
Q

Describe the zones of a burn

A

Zone of coagulation - this occurs at the point of maximum damage. Here there is irreversible loss of tissue due to coagulation of constituent proteins

Zone of stasis - decreased tissue perfusion, tissue is potentially salvageable. Burns resuscitation will increase tissue perfusion

Zone of hyperaemia - outermost area, tissue perfusion, tissue will recover

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11
Q

What are the systemic responses and what is the body burn percentage required?

A 
30% of total body surface area - release of cytokines 
Peripheral vasoconstriction
Myocardial contractility 
Systemic hypotension
Bronchoconstiction
Increased basal metabolic rate
Decreased regulation of immune response
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12
Q

How does a blister occur?

A

Mechanical fatigue of the epidermis
Fatigue causes a split in the stratum spinosum
Separation and hydrostatic pressure allows a fluid pocket to form in the space
New cells divide in the basal layer to allow repair

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13
Q

Advantages and disadvantages of solid medication

A

Advantages

  • more accurate in a full tablet dose
  • Can have a timed release
  • easier to transport
  • less expensive to produce

Disadvantages

  • harder to swallow, choking hazard
  • lower absorption rate
  • inaccurate for smaller doses
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14
Q

Advantages and disadvantages of liquid medication

A

Advantages

  • easier to swallow
  • can accurately measure small doses using a syringe
  • rapid absorption

Disadvantages

  • specialist equipment required for measurement
  • more expensive to produce
  • taste
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15
Q

Risk factors for atheromas

A 
Increased age
Male 
Strong family history
Smoking
Obesity
Hypertension
Hyperlipidaemia
Diabetes
Genetics
Increased alcohol intake
South Asian or african
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16
Q

What happens in reversible cell injury?

A 
Impaired mitochondrial function
cessation of oxidative phosphorylation
Fall in ATP
impaired functioning of energy dependent Na+ pump
Na+ and water enter the cytoplasm
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17
Q

Define necrosis and describe the range of cellular appearances

A 
Cell death. 
Cytoplasmic changes
- swelling 
- increased eosinophilia
- increased binding to denatured proteins
- Glassy appearance: vacuolation

Nuclear changes

  • dark clumps (PYKNOSIS)
  • fragmentation (KARYORRHEXIS)
  • dissolution (KARYOLYSIS)
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18
Q

Define apoptosis and describe the range of cellular appearances

A

Programmed cell death

Absence of inflammatory tissue reaction - occasionally seen in disease states, can lead to neoplasms

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19
Q

What are the 4 stages of apoptosis?

A
  • Induction: signal transduction, damage to mitochondrial membrane, DNA and cell membrane
  • Effector: signalling and other initiating events integrated by specific proteins, modulation of mitochondrial membrane permeability, accumulation of p53
  • Degradation: activation of caspases, cross-linkage of structural proteins, DNA degradation
  • Phagocytosis: attraction of macrophages, binding of thrombomodulin
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20
Q

What are the different types of necrosis?

A
  • Coagulative: infarcts
  • Liquefactive: infections
  • Caseous: TB
  • Fat necrosis: acute pancreatitis
  • Fibrinoid: immune reaction in vessels
  • Gangrenous: entire limb loses blood supply
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21
Q

Define: atheroma

A

accumulation and swelling in artery walls made up of macrophage cells, debris, lipids, calcium and connective tissue

NO ADIPOSE CELLS - macrophages that have taken up oxidised LDL

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22
Q

What are the 3 steps involved in the formation of atheromas?

A
  1. Fatty streaks develop in the site of stress, monocytes migrate in the intimal wall and absorb lipids
  2. Monocytes become foam cells and die off. Cells from the tunica media stabilise the lipid pod forming a fibrous cap.
  3. Plaque continues to grow, disrupting normal blood flow. It can then become unstable and form a thrombus
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23
Q

Define: infarction

A

Tissue death (necrosis) caused by a local lack of oxygen due to an obstruction of the tissues blood supply

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24
Q

Causes of infarction?

A 
Obstruction
Compression
Trauma
Vasoconstriction
Hypotension
Torsion
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25
Q

What are white and red infarctions?

A

White - affects solid organs. There is arterial obstruction to solid tissues

Red - occlusion of a vein, congested tissues, tissues with dual circulation

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26
Q

What are the 3 principal components of ischemia?

A

Hypoxia
Insufficiency of metabolic substrates
Accumulation of metabolic waste

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27
Q

What are the steps of the ischaemic cascade?

A
  1. Lack of oxygen causes a lack of energy (ATP) so the cell switches to anaerobic metabolism
  2. ATP transport pumps fail and calcium flows into the cell
  3. Increased calcium generates free radicals, reactive O2 species and enzymes
  4. Cell membrane is broken down as are mitochondria
  5. Death of cells and inflammatory response
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28
Q

Describe the structure of a hair

A

Inner - Medulla
Middle - cortex
Outer - cuticle

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29
Q

What are the 5 steps of wound healing?

A

Haemostasis (formation of fibrin blood clot)
Inflammation (removal of bacteria and damaged tissue)
Fibroplasia and angiogenesis (fibroblasts lay down new collagen)
Epithelisation (migration and mitosis of keratinocytes)
Remodelling

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30
Q

Describe a gram negative cell wall

A

Lipopolysaccharide (LPS) on the outer surface with a thin layer of peptidoglycan between the inner and outer layer

Under a gram stain it appears pink

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31
Q

Describe a gram positive cell wall

A

Teichoic acid on the outer surface and a thick layer of peptidoglycan.

Under a gram stain it appears violet.

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32
Q

Define pneumonia and the different types

A

Any infection of lung parenchyma and can result whenever defence mechanisms are impaired.

Community acquired, hospital acquired, aspiration and chronic

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33
Q

What are the bacterial causes for pneumonia?

A 
Steptococcus pneumoniae (most common)
Haemophilus influenzae
Moraxella catarrhalis
Staphylococcus aureus
Klebsiella pneumoniae

Staphylcoccus Aureua (hospital acquired)

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34
Q

What is the difference between lobar and lobular?

A

Lobular - patchy consolidation of the lung

Lobar - consolidation of an entire lobe

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35
Q

What are the 4 stages of the inflammatory response of lobar pneumonia?

A
  1. Congestion (lung is boggy and red, vascular enlargement)
  2. Red hepatisation (confluent exudation of neutrophils and red cells, fibrin fills alveolar space)
  3. Grey hepatisation (disintegration of red cells to grey)
  4. Resolution (consolidated exudate undergoes enzymatic digestion
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36
Q

Streptococcus pneumoniae

A

Gram positive diplococci

Normal flora in 20% of adults

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37
Q

Haemophilus influenzae

A

Gram negative coccobacillus

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38
Q

Staphylococcus aureus

A

Gram positive cocci

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39
Q

Risk factors for pneumonia

A 
Extremes of age
Chronic airway disease
Heart disease
Suppressed immune system
Smoking

Hospital acquired - being on a ventilator, antibiotic use that is prolonged and immunosuppression

Aspiration - dibilitated patients

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40
Q

What are the 4 different types of genetic exchange?

A

Transformation - free DNA taken up by the cell
Transduction - DNA transfer by bacteriophage
Conjugation - transmission of plasmid between 2 bacteria
Transposons - jumping genes

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41
Q

What are the causes and implications of antibiotic resistance?

A

Causes:
INAPPROPRIATE PRESCRIBING

Implications:
Increased infections which are harder to treat
Increased morbidity and mortality
Prolonged hospital stay and complication
Economic cost
Increased patient worry
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42
Q

What are the 4 main routes for infection to enter the CNS?

A

Haematogenous
Direct implantation
Local extension
Transport along peripheral nervous system

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43
Q

What are the main causes of meningitis in the 3 different age groups?

A

Neonates - Escherichia coli & group B streptococcus

Adolescents - neisseria meningitidis

Elderly - streptococcus pneumoniae and listeria monocytogenes

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44
Q

What are the signs of meningitis?

A 
Headache
Photophobia
Irritability
Clouding of consciousness
Neck stiffness
Cloudy CSF
Petechial rash (only in neisseria meningitidis)
Sudden onset
Positive Kernigs
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45
Q

What causes cloudy CSF in meningitis?

A

Increased neutrophils
increased protein
decreased glucose

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46
Q

What vaccines are available for meningitis?

A

A and C

No B

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47
Q

Neisseria meningitidis

A

Gram positive diplococcus

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48
Q

Escherischa Coli

A

Gram negative baccilus

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49
Q

Group B streptococcus

A

Gram positive streptococcus

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50
Q

Listeria monocytogenes

A

Gram positive baccilus

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51
Q

What is the mechanism of antibiotic hypersensitivity?

A

Type 2 hypersensitivity
Beta lactam ring forms bonds with the body self proteins
It binds to erythrocytes forming a HAPTEN
This elicits TH2 response
IgE antibodies to self
Causes haemolytic anaemia

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52
Q

Public health protocol for meningitis?

A

Contacts are trace
Information is given to schools and universities
Cases referred to hospital quickly
Cases are investigated properly
Referred to disease control
Notify the HPA
Chemoprophylaxis is given if they have lived in the same household for a week

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53
Q

Chemoprophylaxis for meningitis?

A

Rifampicin

Ciprofloxacin

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54
Q

Define: strict pathogen

A

not found in normal flora

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55
Q

Define: opportunistic infection

A

normal flora that cause disease when given to unprotected sites

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56
Q

Define: faculative pathogen

A

can grow and survive in the environment as well as the host

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57
Q

How can viruses be categorised?

A

Enveloped vs naked
Single strand vs double strand
Positive sense vs negative sense
DNA vs RNA

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58
Q

Limitations of antivirals

A 
few drugs are available
drug resistance
high mutagenic rate
latent and persistent infections
other interactions causing side effects
expensive
adherence to medication
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59
Q

How is varicella zoster spread?

A

aerosol or direct contact

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60
Q

Describe the infection pattern of VZV

A

Primary infection in childhood
Can be reactivated in later life
VZV perrsists in the dorsal root ganglion of sensory nerves

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61
Q

Clinical features of VZV (chicken pox)?

A 
burning discomfort in dermatome
discrete vesicles after 3-4 days
brief viraemia
severe prolonged rash
thoracic dermatomes most common, however can be opthalmic
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62
Q

Varicella Zoster Virus

  • transmission
  • virus structure
A

Herpes virus
Double stranded DNA virus, capsulated
Highly cell associated and attached to proteoglycan on cell surface
transmitted via the respiratory route and direct contact

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63
Q

Epidemiology of VZV

A

Epidemics more prevalent in temperate climates
Epidemics occur in later winter and spring

Varicella between 5 and 10 years
incidence = birth rate
Zoster - 3/1000/year most common in over 45s

More common in those with immunosuppression, leukaemia, steroid therapy.

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64
Q

Pathogenesis of varicella zoster virus

A
  • Primary viraemic stage - virus travels to regional lymph nodes and liver for incubation period (14 days)
  • Secondary viraemic stage - spread to skin and mucous membranes and viral release into the respiratory system
  • Maculopapular phase - vasculitis and fusion of epithelial cells. Also affects cells of lymphatic vessels
  • Vesicular phase - ballooning degeneration of epithelial cells, fluid fills spaces between cells
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65
Q

Consequences of inadequate body response to VZV

A

Varicella pneumonia (infection of alveoli and inadequate oxygen transfer)

  • Transient hepatitis (extensive viral replication in the liver and hepatocellular destruction)
  • Varicella encepholitis
  • Cerebellar ataxia
  • Thrombocytopaenia
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66
Q

Clinical features of varicella zoster (shingles)

A

Localised, puritic, vesicular rash in 1-2 dermatomes
Progression to large fluid filled lesions
Localised neuropathic pain
Severe pain (can last longer than rash)

67
Q

Prophylaxis for shingles/chicken pox?

A

Difficult due to infection 2 days before symptom onset
Infected patients must be treated in isolation
IgG is given if immunocompromised or pregnant
Acyclovir (must be given within 3 days after rash onset)

68
Q

Cause of infectious mononucleosis

A

Epstein Barr Virus (90%)

Cytomegalovirus (10%)

69
Q

Epstein Barr Virus

A

Transmitted by close human contact (saliva)
Enveloped
DNA virus

70
Q

Pathogenesis of infectious mononucleosis

A
  • Infection begins in nasopharyngeal and oropharyngeal lymphoid tissue and spread to epithelium and submucosa
  • EBV envelope binds to B cells
  • Latent infection
  • B cell activation and proliferation
  • B cells disseminate and secrete antibodies
  • Reactive T cell proliferation causes enlargement of lymphoid tissue
71
Q

Presentation of glandular fever

A 
low grade fever
fatigue/ prolonged malaise
sore throat
enlarged tonsils
fine macular, non-prutic rash
bilateral upper lid oedema
lymphadenopathy
nausea
anorexia
mild hepatomegaly and splenomegaly
72
Q

What areas of the brain are responsible for temperature regulation? What is required to raise the set point?

A

Preoptic and anterior hypothalamic nuclei

Prostaglandin E2

73
Q

What is responsible for temperature regulation?

A
  • dermal blood flow
  • pili erector muscles
  • eccrine sweat glands
  • dermal thermoreceptors
  • skeletal muscle (shivering)
  • hypothalamus
  • adipose tissue
  • sympathetics
74
Q

Different types of fever

A

Continuous (no more than 1oC fluctuation in a day)
Intermittent (malaria)
Remittent (always present but less than 1oC fluctuation)
Hepatic/septic (steep fluctuation, septicaemia)
Pel Ebstein (recurrent bouts, glandular fever)
Low grade (<37.8)

75
Q

How are communicable diseases controlled?

A

Surveillance
Preventative measures
Outbreak investigation
Control measures

76
Q

Define: epidemic

A

occurrence in a community or region of cases of an illness or other health related events clearly in excess of normal expectancy

77
Q

Define: outbreak

A

epidemic limited to localised increases in the incidence of a disease e.g. a town

78
Q

Define: pandemic

A

epidemic occurring over a very wide area, crossing international boundaries and affecting a large number of people e.g. swine flu

79
Q

What is a notifiable disease and give 3 examples and give procedures involved in preventing the spread

A

legal obligation to report to HPA
MRSA, C. Difficile and MSSA
screening of patients, barrier nursing (treating infected in isolation), sharp disposal, decontamination and sterilisation of instruments and HAND WASHING

80
Q

Epidemiology of HIV

A 
8% adults in sub-saharan africa
Homosexuals (50% and decreasing)
Intravenous drug users (20%)
Haemophiliacs (0.5%)
Recipients of blood or components (1%)
Heterosexual contacts of those in high risk group (10%)
Undetermined (5%)
Paediatric (from mother to baby = 2%)
81
Q

Methods of transmission for HIV

A
  • Sexual transmission (75%) carried in semen and enters through mucosal abrasions. It is also present in viral secretions and cervical cells
  • Parenteral transmission in 3 groups. Intravenous drug users, haemophilacs who received factor 8 and 9, recipients of blood transfusions
  • mother to infant transmission via 3 routes. In utero via placental spread, during delivery through infected birth canal, after birth through breast milk
82
Q

Human Immunodeficiency Virus

A

RNA Retrovirus from the lentivirus family
Nucleocapsid protein p7
2 copies of RNA
3 viral enzymes - protease, reverse transcriptase, integrase)
Matrix protein around core p17
2 viral glycoproteins - gp41 and gp120

83
Q

Describe HIV entry and replication

A

HIV enters through mucosal tissues and blood and infects T cells, dendritic cells and macrophages.

  1. GP120 on HIV attaches to CD4 receptor
  2. Conformational change
  3. GP120 and CD4 receptor binds to CCR4 (chemokine receptor)
  4. GP41 penetrations
  5. membrane fusion
  6. RNA genome enters the host
  7. Reverse transcriptase creates proviral DNA
  8. It is integrated into the host genome
  9. Replication of proteins and forms virions for release
84
Q

What cells do HIV infect?

A

T cells
memory and activated
NOT naive

85
Q

In HIV infection how are T cell numbers reduced?

A

Direct killing of infected cells
Viral replication interfering with protein synthesis
HIV colonises in lymph glands causing the destruction of lymphoid tissue
Infection of thymic progenitor cells
Fusion of infected and uninfected cells (giant cells)
Infection of accessory calls that secrete cytokines for CD4 maturation

86
Q

What is the role of macrophages in HIV infection?

A

They can be infected and allow viral replication however they are resistant to cytopathic effects.
Reservoirs of infection
HIV can be carried to the brain by macrophages

87
Q

Stages of HIV infection

A
  1. Acute retroviral syndrome
    Primary infection of cells, travels to lymph cells and infection becomes established in lymphoid cells. Occurs 3-6 weeks after infection and resolves within 2-4 weeks. Viraemia. Non specific illness - sore throat, fever, weight loss, diarrhoea, fatigue.
  2. Latency/ middle chronic phase
    Asymptomatic, low levels of infection. Provirus in host DNA
  3. Activation by microbial infections or cytokines leading to extensive viral replication and CD4 cell lysis
  4. AIDS - depletion to CD4 cells
88
Q

How is HIV infection classified?

A

Asymptomatic or symptomatic
CD4+ levels/ microlitre
>500, 200-500, <200

89
Q

What are some of the AIDS defining opportunistic infections?

A

FUNGAL INFECTIONS - candidiasis, pneumocytosis, histoplasmosis, cryptococcus
VIRAL - cytomegalovirus, herpes simplex, VZV
BACTERIAL - norcardiosis, salmonella infections

90
Q

Factors that inform decision to treat HIV

A
  • recent exposure (last 72 hours) PEP
  • CD4 below 350
  • CD4 at 500 with hep B or C
  • Radiotherapy
  • Chemotherapy
  • TB
  • HIV related nephropathy
91
Q

Risk factors for fungal infections

A 
Broad spec antibiotics
Immunocompromised
Corticosteroid treatment
Radiotherapy
Intensive care
Extremes of age
Pregnancy
Cancer
92
Q

What is HAART and what components are used?

A

Highly active AntiRetroviral Therapy
2 nucleoside reverse transcriptase inhibitors
with non nucleoside reverse transcriptase inhibitors
OR 1 or 2 protease inhibitors

It inhibits HIV replication and RNA is reduced to undetectable levels. Survival is prolonged however the regimen is complex and has many side effects. Compliance is difficult and treatment is life long.

93
Q

What are the UK standard vaccinations given to children under 6 months?

A 
Rotavirus gastroenteritis
Diptheria
Tetanus
Pertussis
Polio
HIB (haemophilis influenza B)
Meningitis C
94
Q

What are the UK standard vaccinations for children above 1 year?

A

MMR
HPV
Boosters for DTP/Polio/MenC

95
Q

What are the vaccinations that are given to adults?

A

Shingles (70&79)
Influenza (if high risk group of over 65)
Pertussis (pregnancy between 28 and 38 weeks)
Pneumococcal vaccination for pneumonia and meningitis for over 65s and high risk groups
Hep B if working with blood products
TB if born in high risk area

96
Q

What are the different types of vaccinations?

A
  • Inactivated e.g. pertussis
  • Live attenuated e.g. measles, mumps
  • Inactivated vaccines
97
Q

Advantages and disadvantages of live attenuated vaccines?

A

Advantages

  • strong cellular and antibody response
  • lifelong immunity with 1 or 2 doses

Disadvantages

  • can revert to virulent form
  • can’t be given to those with low immune systems
  • must be kept refridgerated
98
Q

Advantages and disadvantages of inactivated vaccines?

A

Advantages

  • More stable and safer
  • Easily transported and stored

Disadvantages

  • weaker immune response
  • boosters required
99
Q

What are the 3 morphological classifications of fungi?

A

Moulds
Yeasts
Dimorphic

100
Q

What are the features of a mould?

A
  • growth by formation of filaments of HYPHAE

- reproduce asexually through asexual spores or sexually

101
Q

What are the features of a yeast?

A
  • single celled organisms that are round or ovoid
  • reproduce by budding
  • some form elongated buds (pseudohyphae)
102
Q

Cervical cancer is caused by a virus (which one)?

A

HPV 16 and 18

103
Q

What is the function of viral proteins E6 and E7 in cervical cancer?

A

E6 - induces rapid degeneration of p53 via ubiquitin dependent proteolysis
E7 - complexes with the active form of RB, protmoting proteolysis via proteosome pathway

104
Q

What is the definition of a HSIL (high grade squamous intraepithelial lesion) and LSIL?

A

LSIL - atypical immature squamous cells confined to lower 1/3 of epithelium

HSIL - expanded to 2/3 or epithelial thickness

105
Q

How is cervical cancer treated?

A

Microinvasive - cone biopsy
More invasive - hysterectomy
Most advanced - irradiation

106
Q

Describe the lesions found in eczema?

A

red, papulovesicular, oozing and crusted lesions.

If it persists - raised scaling plaques due to hyperkeratosis

107
Q

What are the different types of dermatitis?

A
  • allergic contact
  • atopic
  • drug related
  • photoeczematous
108
Q

Pathophysiology of eczema?

A
  • triggered by contact allergens
  • antigens are taken up by dendritic langerhans cells
  • migrate using dermal lymphatics to lymph nodes
  • presented to naive CD4 t cells which are activated and produce memory cells
  • on reexposure memory T cells migrate to affected skin sites
  • adhere to postt capillary venules, extravastate into tissues and release cytokines and chemokines that recruit inflammatory cells
109
Q

What are the different types of skin cancer?

A

Squamous cell carcinoma
Basal cell carcinoma
Melanoma

110
Q

Features of a squamous cell carcinoma?

A
  • discovered while small
  • less than 5% metastasise
  • deeply invasive, involve subcutis
111
Q

What are the 2 main causes of squamous cell carcinoma?

A

DNA damage induced by UV light

Chronic immunosuppression

112
Q

What is the role of p53 in cancer?

A
  • damage to cells
  • check point kinases ATM and ATR sense the damage
  • They upregulate expression and stability of p53
  • p53 arrests cells in G1
    Promotes DNA repair or cell elimination

p53 dysfunction loses this protective function and is an early event in the development of cancer

113
Q

Presentation of skin cancer - squamous cell carcinoma?

A

early
scaly or crusty area of skin or lump
red inflamed base
often tender

114
Q

Risk factors for squamous cell carcinoma?

A 
older people
people who work outdoors
fair skin
UV light treament
immunosuppression
115
Q

Features of basal cell carcinoma?

A
  • invasive
  • slow growing
  • rarely metastasise
  • increased in sun exposed sites
116
Q

Presentation of basal cell carcinoma?

A
  • pearly papules often containing prominent dilated epidermal blood vessels.
  • Some contain melanin
  • Advanced lesions may ulcerate
117
Q

Features of a melanoma?

A
  • Evolve over time from localised skin tumours to aggressive tumours that metastasise and are resistant to therapy
  • early recognition vital
118
Q

Presentation of a melanoma?

A
  • usually asymtomatic
  • lesions >10mm in diameter
  • Changes in colour, size and shape of pigmented lesion
  • Variations of colour
  • Asymmetry
  • Borders (irregular)
  • Colour (variegated)
  • Diameter
  • Elevated
119
Q

Define Breslow thickness

A

the distance from the superficial epidermal layer to the deepest intradermal tumour cells

120
Q

Risk factors for melanoma

A
  • sun exposed surfaces
  • lightly pigmented individuals
  • 15% familial
  • Female
  • Family history
121
Q

Pathogenesis of melanoma

A

Mutation that diminish the activity of RETINOBLASTOMA (RB) tumour suppressor proteins
P16 enhances activity of RB

30-70% of melanomas involves the loss of p16

Alterations in genes = increased melanocytic proliferation = escape from oncogene induced cellular senescence

122
Q

How is cancer classified/ tumour staging?

A

TNM staging
T - size of original tumour and whether it has invaded nearby tissue (0-4)
N - any nearby lymph nodes involved (0-3)
M - metastasis (0-1)

123
Q

What are the 5 mechanisms of cancer spread?

A
  1. Transcoelomic - seeding the surface of peritoneal, pleural, pericardial or subarachnoid spaces e.g. surgical manipulation
  2. Lymphatic spread
  3. Haematogenous
  4. Implantation
  5. Local
124
Q

What are the 8 hallmarks of cancer?

A
  1. Self sufficiency in growth signals (oncogenes)
  2. Insensitivity to anti-growth signals (tumour suppressors)
  3. Evasion of apoptosis
  4. Limitless replicative potential (telomerase)
  5. sustained angiogenesis
  6. tissue invasion and metastasis
  7. reprogramming of energy metabolism
  8. evasion of immune destruction
125
Q

Define oncogenes

A

genes whose presence can trigger development of cancer

126
Q

Define tumour suppressor genes

A

genes whose loss or inactivation can trigger development of cancer

127
Q

Define macule

A

flat mark on the skin

Can be pigmented like a freckle or red as in capillary haemangioma

128
Q

Define papule

A

small solid elevation of the skin <5mm in diameter

129
Q

Define nodule

A

papule >5mm can be oedematous or solid

130
Q

define vesicle

A

small blister <5mm

consists of clear fluid within/below the epidermis

131
Q

Define cyst

A

nodule consisting of an epithelial lined cavity filled with fluid or semisolid material

132
Q

Define plaque

A

palpable plateau like elevation of normal skin

133
Q

Define purpura

A

extravastation of blood, red, discolouration of skin

134
Q

How are cancer changes analysed?

A
  • Histochemical stains
  • Immunohistochemical stains
  • Flow cytometry
  • Cytogenetics
  • FISH
  • PCR
135
Q

What is FISH?

A

Fluorescent in situ hybridisation

Uses special fluorescent dyes linked to pieces of DNA that can only attach to specific parts of certain chromosomes

Can show gene amplification

136
Q

How can flow cytometry analyse cancer changes?

A

Tests cells from bone marrow, lymph and blood

Cell sample is treated with antibodies and passed in front of a laser beam. If sample contains antigens then the laser will make them give off light

Can be used to measure the amount of DNA in cancer cells

137
Q

What are the risk factors for cervical cancer?

A 
multiple sexual partners
promiscuous male partner
young age at first intercourse
high parity
persistent infection with HPV
use of oral contraceptives
smokers
immunosuppression
138
Q

How is a squamous intraepithelial lesion diagnosed?

A 
nuclear atypia
nuclear enlargement
hyperchromasia
coarse chromatin granules
variation in nuclear size or shape
cytoplasmic halos
139
Q

What are the different types of cervical cancer and how common are they?

A 
Squamous cell carcinoma (80%) = HSIL precursor
Cervical adenoma (15%) = adenocarcinoma in situ precursor
Adenosquamous and neuroendocrine = 5%
140
Q

How often is a pap smear carried out?

A

25 years upwards - every 3 years
Over 50 years - every 5 years

10% false positive

141
Q

What vaccinations are given at 2 months?

A

5 in 1 - dipetheria, tetanus, pertussis, polio, haemophilus influenzae
Pneucococcal vaccine
Rotavirus gastroenteritis

142
Q

What vaccinations are given at 3 months?

A

5 in 1 (2nd dose) - diptheria, tetanus, pertussis, polio, haemophilus influenzae
Meningitis C
Rotavirus

143
Q

What vaccinations are given at 4 months?

A 
5 in 1 (3rd dose) - diptheria, tetanus, pertussis, haemophilius influenza, polio
pneumococcal vaccine (2nd dose)
144
Q

What vaccinations are given at 1 year?

A

Haemophilus influenza B (4th)
Meningitis C (2nd)
MMR
Pneumococcal (3rd)

145
Q

What vaccinations are given at 3 1/2 years?

A

MMR (2nd)

preschool booster 4 in 1 = diptheria, tetanus, pertussis, polio

146
Q

What vaccinations are given at 12-13 years?

A

HPV

147
Q

What vaccinations are given from 13-18 years?

A

Polio booster

Men C booster

148
Q

What is leukaemia?

What are the common features?

A

neoplastic proliferations of white blood cell precursors

Diffuse replacement of normal bone marrow by leukaemic cells with variable accumulation of abnormal cells in the peripheral blood
Bone marrow failure leading to anaemia, neutropaenia, thrombocytopaenia

149
Q

What are the features of acute leukaemia?

A

Leukaemic cells don’t differentiate
Bone marrow failure
Rapidly fatal if untreated
Potentially curable

150
Q

What are the features of chronic leukaemia?

A

Leukaemic cells retain the ability to differentiate
Proliferation without bone marrow failure
Survival for a few years
Not curable without bone marrow transplant

151
Q

Describe how acute leukaemia occurs?

A

Arises from mutations in haemopoietic stem cells. These cells proliferate but lose the ability to differentiate into mature blood cells.
It leads to an accumulation of blast cells in the bone marrow and thus bone marrow failure.

152
Q

What are the clinical features of acute leukaemia?

A

They reflect inadequate haematopoiesis secondary to bone marrow infiltration
Anaemia - SOB, tiredness, weakness
Leukopaenia - recurrent infections
thrombocytopaenia - bleeding and bruising
Marrow infiltration - bone pain

153
Q

What are the 2 types of acute leukaemia?

A 
Acute myeloid (myeloblastic) leukaemia AML
Acute lymphoid (lymphoblastic) leukaemia ALL
154
Q

Describe AML

A

acute myeloid leukaemia
median age of presentation is 65 years
may arise with unknown aetiology or related to cytotoxic chemotherapy
must have at least 20% blast cells in bone marrow for diagnosis

155
Q

Describe ALL

A

acute lympohoid leukaemia
most common between 2-4 years and is the most common cause of childhood cancer
majority of cases arise from B cell precursors

156
Q

What are the clinical features of chronic leukaemia?

A 
symptomatic anaemia
abdominal discomfort
splenomegaly
weight loss
fever
sweats
157
Q

What are the 2 different types of chronic leukaemia?

A

chronic myeloid leukaemia CML

chronic lymphocytic leukaemia CLL

158
Q

Describe CML

A

occurs in all age groups
median survival of 5 years
normal bone marrow replaced with clone derived from pluripotent stem cell (philadelphia chromosome)
Erythoid, megakaryocytic and B lymphocytes all carry the defect as well as the granulocytes

159
Q

Describe CLL

A

occurs predominantly in later life 65-67 years
most common leukaemia and occurs in B cells (95%)
Median survival of 25 years and generally does not require therapy
Can have either: naive B cell blasts (shortened prognosis) or fully functioning B cell blasts

160
Q

Name some bio mechanical markers of cell death?

A

Creatine kinase - muscles
Troponins - cardiac muscle
ALT - liver

161
Q

What happens in irreversible cell death?

A

Lysosomal contents leaks into cytoplasm
Enzymatic digestion of cell constituents
Cell components leak into extra cellular space

162
Q

Define thrombosis

A

Formation of clot from blood constituents with vascular system

163
Q

Risk factors for thrombus formation?

A 
Age
Immobilisation
Trauma
Surgery
Cancer
Pregnancy
Oral contraceptive
Smoking
Radiation
Heart disease

Year 2 - Theme A (7 decks)

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